Clinical and experimental skeletal muscle alcoholic myopathy

1988 ◽  
Vol 16 (3) ◽  
pp. 250-251 ◽  
Author(s):  
T. J. PETERS ◽  
R. J. WARD ◽  
P. DUANE ◽  
V. R. PREEDY
2018 ◽  
Vol 38 (1) ◽  
pp. 197-217 ◽  
Author(s):  
Scot R. Kimball ◽  
Charles H. Lang

Both acute intoxication and longer-term cumulative ingestion of alcohol negatively impact the metabolic phenotype of both skeletal and cardiac muscle, independent of overt protein calorie malnutrition, resulting in loss of skeletal muscle strength and cardiac contractility. In large part, these alcohol-induced changes are mediated by a decrease in protein synthesis that in turn is governed by impaired activity of a protein kinase, the mechanistic target of rapamycin (mTOR). Herein, we summarize recent advances in understanding mTOR signal transduction, similarities and differences between the effects of alcohol on this central metabolic controller in skeletal muscle and in the heart, and the effects of acute versus chronic alcohol intake. While alcohol-induced alterations in global proteolysis via activation of the ubiquitin-proteasome pathway are equivocal, emerging data suggest alcohol increases autophagy in muscle. Further studies are necessary to define the relative contributions of these bidirectional changes in protein synthesis and autophagy in the etiology of alcoholic myopathy in skeletal muscle and the heart.


2021 ◽  
Vol 26 (4) ◽  
pp. 23-30
Author(s):  
N. S. Shcheglova ◽  
E. O. Zinovyeva ◽  
B. S. Shenkman

In Russia, there is a high level of alcohol consumption among women in doses that represent a high risk of developing alcoholic diseases, manifested, in particular, by damage to skeletal muscles.The purpose of the study. Analysis of clinical, biochemical, neurophysiological, as well as morphometric and immunohistochemical features of alcoholic skeletal muscle damage in women with chronic alcohol intoxication.Material and methods. A clinical and laboratory examination of 30 women aged 20 to 60 years with chronic alcohol intoxication was performed, which included the determination of creatine phosphokinase (CPK) and insulin-like growth factor I (IGF-I) in blood plasma, stimulation and needle electromyography (EMG), as well as morphological and immunohistochemical examination of biopsies of the quadriceps femoris.Results. Myopathic syndrome in the form of proximal para-or tetraparesis was observed in 73.3% of the examined women in combination with a decrease in IGF-1 at normal values of CPK in blood plasma. The EMG results indicated the absence of changes in the parameters of the potentials of motor units, characteristic of primary muscular lesions, and of conduction disturbances along the femoral nerve. Morphometric and immunohistochemical studies of skeletal muscle biopsies showed a decrease in the cross-sectional area of muscle fibers of types I and II without signs of muscle tissue necrosis.Conclusion. Chronic alcoholic myopathy is a common manifestation of alcoholic disease in women with long-term alcohol intoxication. The severity of the atrophic process in the skeletal muscle is comparable to the degree of proximal paresis. Violations of systemic protein synthesis and acceleration of apoptosis are considered as pathogenetic mechanisms of the atrophic process in the muscles in chronic alcoholic myopathy in women.


1999 ◽  
Vol 5 (S2) ◽  
pp. 1162-1163
Author(s):  
B. Müller ◽  
H.J. Finol ◽  
I. Montes de Oca ◽  
A. Mayorca.

Two forms of muscular alterations have been described in alcoholic patients, one acute, the so called Hypokalemic alcoholic Myopathy; focal or diffuse pain, swelling, tenderness and weakness of skeletal muscle are the main clinical features, and the chronic one with proximal muscle weakness wich progresses slowly in a period of weeks or months Ultrastructurally myofibril disorganization and necrosis where described.In this work we present a systematic study of skeletal muscle alterations in four alcoholic patients who attended the Department of Internal Medicine at Caracas University Hospital . The patients were males, ages between 56 and 62 years old, and presented chronic alcoholism with muscle weakness with a more distal distribution and polymyalgia. Biopsies were taken from quadriceps femorismuscle with a percutaneous neddle and processed for routine transmission electron microscopy.Muscle fibers showed different degrees of atrophy with myofibril disorganization (Fig.l) and disappearence (Fig.2). Myonuclei were hyperchromatic and intermyofibrilar spaces were widened and exhibited abundant lipid droplets.


1979 ◽  
Vol 301 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Howard L. Bleich ◽  
Mary Jean Moore ◽  
Emanuel Rubin

Author(s):  
Wang Nan ◽  
Oleksandr Motuziuk

Myopathy of the skeletal muscles is caused by excessive misuse of ethanol and affects half to two-thirds of pathological alcohol abusers. It is possible to identify alcohol-induced skeletal muscle disruptions as either 'acute or chronic'. Medium to moderate alcohol has positive or defensive effects (such as cardiovascular) on some organ systems, but long-term drinking and acute toxicity can adversely impact multiple organ systems and potentially increase mortality. Therefore we need a detailed understanding of the study status of alcoholic myopathy. References for researching alcoholic myopathy can be given by the review of this article.Search the Web of Science (WOS) central archive for alcoholic myopathy research papers from 2000 to 2020, and use CiteSpace and WOS databases for their own literature statistics techniques to evaluate the number of written articles, research organizations, citations to literature and identification of keywords.A total of 947 publications were collected after screening and the number of articles published grew year by year. The average number of released publications is 47.355. Most documents have been released by a total of 7 countries. Among them, 397 papers were published by the US, ranked first among all nations. Its intermediate centrality is also the largest, suggesting that other countries have more recognition of its scientific findings. The papers published by Emory Univ and Kobe Univ are well regarded in the field, among the top 7 academic institutions with publication volumes. There are 28 core authors and a total of 263 written articles. Highly cited papers are classified into 40 categories, of which 11 are prominently clustered categories. Co-occurrence study of keywords reveals that keywords such as skeletal muscle, oxidative stress, ethanol, alcohol, etc. are very common. The literature on alcoholic myopathy is primarily focused in Western countries, and autophagy, ROS and antioxidants are the latest study hotspots.


1987 ◽  
Vol 73 (6) ◽  
pp. 601-603 ◽  
Author(s):  
P. Duane ◽  
T. J. Peters

1. Chronic alcoholism is associated with a selective atrophy of type II skeletal muscle fibres. We studied the glucocorticoid status of chronic alcoholics with and without myopathy to determine if hypercortisolism is responsible for the myopathy. 2. Twenty-four hour urinary Cortisol excretion and diurnal serum Cortisol measurements were not significantly different in chronic alcoholics, with and without atrophy of type II skeletal muscle fibres. 3. Diurnal serum Cortisol variation was normal for both groups of alcoholics studied. None of the patients with myopathy had raised serum Cortisol levels. 4. We conclude that chronic alcoholic myopathy is not due to alcohol-related pseudo-Cushing's syndrome.


Author(s):  
Danielle E. Levitt ◽  
Patricia E. Molina ◽  
Patricia E.Molina Simon

Skeletal muscle dysfunction is highly prevalent and is one of the earliest pathological tissue changes among people with at-risk alcohol use. Clinical studies to elucidate pathophysiological mechanisms of alcohol-mediated muscle disease are hampered due to ethical considerations, and confounded by nutritional, lifestyle, and comorbid conditions. Rodent models have been developed to study the impact of at-risk alcohol consumption and alcohol-mediated end organ injury, including skeletal muscle dysfunction. This review discusses results from well-established rodent models of alcohol administration and highlights key pathophysiological mechanisms underlying alcoholic myopathy identified in rodent models. Salient pathways include impaired regenerative capacity, altered anabolic/catabolic balance, impaired mitochondrial bioenergetic function, and skeletal muscle morphological and contractile changes.


1985 ◽  
Vol 68 (6) ◽  
pp. 693-700 ◽  
Author(s):  
Finbarr C. Martin ◽  
Timothy J. Peters

1. Muscle protein breakdown in vivo has been studied by measurements of urinary 3-methylhistidine/creatinine ratios. No differences were found between control subjects and chronic alcoholics either with or without proximal muscle wasting or cirrhosis. 2. Calculation of muscle turnover rates, with the correction of Afting et al. (1981, Biochemical Journal, 200, 449-452) for non-skeletal muscle contributions of 3-methylhistidine and creatinine, showed lower values for alcoholics compared with controls. 3. Tissue activities of a neutral protease, assayed by a novel, rapid and sensitive fluorimetric method, were similar in patients and controls. The activity did not vary with severity of atrophy or the presence of cirrhosis. 4. No evidence was therefore obtained to suggest that alcoholic myopathy is due to increased muscle breakdown.


2019 ◽  
Vol 49 (4) ◽  
pp. 490-494
Author(s):  
B. S. Shenkman ◽  
O. E. Zinovyeva ◽  
S. P. Belova ◽  
T. M. Mirzoev ◽  
N. A. Vilchinskaya ◽  
...  

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